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year 3 tcds > COPD > Flashcards

COPD Flashcards

1
Q

What investigations would you perform if suspecting COPD? What would they show?

A
  • Spirometry (to observe if there’s reversibility) -> obstructive or restrictive lung disease; reversibility by bronchodilator (I.e. in asthma)
  • Chest x-ray -> signs of infection, pulmonary oedema, hyper-inflation, emphysema
  • ECG -> ischemic heart disease, arrhythmia, R sided heart strain secondary to underlying lung pathology
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2
Q

What are the hallmark features of COPD?

A
  1. Shortness of breath
  2. Chronic cough
  3. Sputum production
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3
Q

Name causes of COPD

A

Host:
- genetic susceptibility (eg. α1-anti-trypsin deficiency)
- other gene polymorphisms (eg. matrix metalloproteinases, TNF – α
glutathione S transferase)

Environment:

  • tobacco smoke exposure
  • cannabis
  • other smokes
  • mineral dusts (eg coal, cadmium)
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4
Q

What is the pathophysiology of COPD?

A
  1. Inflammation
  2. Goblet cell hyperplasia -> cough + sputum
  3. Airway narrowing -> breathlessness + wheeze
  4. Alveolar destruction -> breathlessness

Fibroblast -> Fibrosis -> obstructive bronchiolitis -> COPD
CD8+ T-cells -> emphysema -> COPD
Protease -> mucus hyper-secretion -> COPD

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5
Q

What are the typical symptoms of COPD?

A
  • Smoker or ex-smoker aged > 35
  • exertional breathlessness
  • chronic cough
  • regular sputum production
  • winter exacerbations
  • wheeze
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6
Q

What are the signs of COPD?

A
  • tar-staining of fingers
  • central cyanosis (if hypoxic or polycythaemic)
  • tachypnoea
  • chest hyperexpansion ‘barrel-shaped’
  • reduced lateral and increased vertical chest expansion Ø paradoxical lower chest motion
  • reduced breath sounds
  • wheeze
  • palpable liver edge
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7
Q

What FEV1/FVC ratio is indicative of obstructive lung disease (I.e. COPD)?

A

FEV1/FVC < 0.7

  • No correction with bronchodilators
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8
Q

How is COPD severity scored?

A

GOLD scale = Global strategy for Obstructive Lung Disease

Stage 1: FEV1 ≥ 80% predicted
Stage 2: 50-79%
Stage 3: 30-49%
Stage 4: ≤ 30%

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9
Q

What is seen on a chest x-ray in a patient with COPD?

A

Often normal x-ray

  • Hyper-inflated lungs
  • Flattened/low diaphragm
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10
Q

What is seen on a CT scan in someone with COPD?

A
  • “holes” or bullae

- Bronchial wall thickening

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11
Q

What happens to the blood gases in type 1 and type 2 respiratory failure?

A 
Type 1:
pH = normal
pCO2 = normal
pO2 = low
HCO3 = normal
Type 2: Respiratory Acidosis
pH = low
pCO2 = high
pO2 = low
HCO3 = high
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12
Q

What is the natural history of COPD?

A
  1. Progressive decline in lung function
  2. Progressive dyspnea and disability
  3. R ventricular failure
  4. Exacerbation
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13
Q

How does R ventricular failure (Cor Pulmonale) develop in COPD?

A
  1. Hypoxia
  2. Pulmonary arterial vasoconstriction
  3. Increased pulmonary artery pressure
  4. R ventricular hypertrophy
  5. R ventricular failure
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14
Q

What is the treatment for COPD?

A
  1. Lifestyle advice -> Stop smoking!
  2. Inhaled bronchodilators
    - used for symptom relief and reduce exacerbations
    - SABA (short-acting b-agonists) = salbutamol, terbutaline
    - LABA (long-acting b-agonists) = salmeterol, eformoteral
    - Anti-muscarinics = ipratropium, tiotropium
  3. Inhaled corticosteroids
    - Reduced exacerbation frequency (if > 2/yr)
    - Slows disease progression?
    - Only used for severe/frequent exacerbations (if FEV1 < 50%)
    - I.e. Beclomethasone, Budesonide, Fluticasone
  4. Oral theophylline
    - Bronchodilator with narrow therapeutic window
    - I.e. aminophylline
  5. Mucolytics (i.e. carbocystine)
    - Reduced mucus production
  6. Surgical procedures
    - bullectomy
    - Lung volume reduction surgery
    - Lung transplantation
  7. End-of-life care
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15
Q

What are some complications of COPD?

A
  1. Exacerbations
  2. Pneumonia
  3. Pneumothorax
  4. R ventricular failure (Cor Pulmonale)
  5. Peripheral neuropathy
  6. Cachexia
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16
Q

How would you treat an acute exacerbation of COPD in hospital?

A
  • Oxygen (give to maintain SpO2 between 88-92%)
  • High dose SABAs usually nebulised (I.e. salbutamol)
  • High dose corticosteroids (prednisolone 40mg/day for 7d)
  • Antibiotics If purulent sputum or very severely ill
  • Reassess after 1h: if still respiratory acidosis then consider all of the following
    1. IV bronchodilator (salbutamol or theophylline)
    2. Urgent intensive care opinion
    3. Non-invasive ventilations
    4. Intubation + assisted ventilation (I.e. CPAP)
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17
Q

Outline the 3 lung function tests

A
  1. Spirometry -> measures the amount of air volume that you breathe in and out
    - VC = vital capacity ~ FVC (forced vital capacity
    - VC = volume of air that you can exhale after a full inspiration. FVC = volume of air you can forcibly exhale after the deepest breath possible. Usually very similar.
    - FEV1 = Volume of air that you can forcibly exhale in 1s
  2. Lung Diffusion Test -> provides info about how well the oxygen that you inhale moves into your bloodstream
    - Inhale CO, hold breath for a few sec, then exhale
    - Inhaled [CO] compared to exhaled [CO]. Results = diffusion capacity of the lungs for CO (DLCO)
    - DLCO < 55% normal value = lungs do NOT efficiently absorb O2
  3. Lung Plethysmography -> determines how much air is in your lungs when you exhale
    - restrictive = difficulty inhaling, while obstructive = difficulty exhaling
    - FRC = how much air is left in the lungs after normal exhalation
    - ERV = additional air forcibly expired after normal expiration (higher than expected in obstructive and decreased in restrictive)
    - TLC = total lung volume
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18
Q

What is the pathophysiology of asthma?

A

Reversible airway obstruction:

  1. Bronchocostriction
  2. Bronchial mucosal oedema
  3. Mucus plugging
    - > Inflammatory response initiated by triggers + mast cell degranulation
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19
Q

Name 3 bronchodilators

A
  1. Synpathomimetic agents
  2. Xanthines
  3. Magnesium
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20
Q

Define COPD

A

Lung disease characterised by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible.

Main features include:

  1. Bronchoconstriction
  2. Mucosal oedema
  3. Mucosal hypersecretion
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21
Q

Describe how sympathomimetic agents act on bronchial smooth muscle

A

B2 adrenoreceptors agonists = activation of SNS = bronchodilation
- ATP turns into cAMP by adenyl cyclise = relaxation of bronchial smooth muscle

Muscarinic ACh receptors = activation of PSNS = bronchoconstriction

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22
Q

Name examples of short-acting and long-acting B2 agonists

A

Short Acting:

  • Salbutamol = ventolin, airomir, salamol easi-breath
  • Terbutaline = Bricanyl

Long-acting:

  • Salmeterol = serevent
  • Formoterol = oxis
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23
Q

List 6 side effects of B2 agonists

A
  1. Tachycardia
  2. Arrhythmia
  3. Myocardial ischemia
  4. Tremor
  5. Paradoxical bronchospasm
  6. Hypokalemia
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24
Q

Describe how anticholinergic drugs work

A

Anticholinergic drugs inhibit bronchoconstriction by antagonising muscarinic receptors of the PNS

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25
Q

Name examples of short-acting and long-acting anticholinergic drugs

A

Short-acting:
- Ipratropium bromide = atrovent

Long-acting:
- Tiotropium = spiriva

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26
Q

What are 3 side effects of anticholinergic drugs? In what conditions should these drugs be used with caution?

A
  1. Dry mouth
  2. Nausea
  3. Headache

Use in caution:

  • Prostatic hyperplasia + bladder outflow obstruction
  • Susceptible to glaucoma
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27
Q

Describe how xanthines work

A

Xanthines are phosphodiesterase inhibitors which raise intracellular cAMP -> increased bronchodilation

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28
Q

List examples of xanthines

A

Theophylline (M/R tablets)

  • Nuelin SA
  • Slo-phyllin
  • Uniphyllin continus

Aminophylline

  • Theophylline + ethylenediamine (increased water solubility allowing IV preparation)
  • Phyllocontin continus (M/R tablet)
29
Q

What are 6 side effects of xanthines? What drug interactions are important to note?

A
  1. Tachycardia
  2. Arrhythmia
  3. Agitation
  4. Convulsions
  5. Hypokalemia
  6. Levels can increase in sepsis + viral infections

Interactions (hepatic metabolism):

  • Ciprofloxacin + OCP reduce clearance of xanthines
  • Anticonvulsants increase clearance of xanthines
30
Q

What anti-inflammatory agents are used in COPD?

A
  1. Corticosteroids
  2. Leukotriene receptor antagonists
  3. Sodium cromoglycate
31
Q

How do corticosteroids work in COPD? List some inhaled, oral, and IV examples

A

Broad anti-inflammatory effect

  • Inhibition of production of inflammatory cytokines
  • Reduced hyper-reactivity of airways

Inhaled:

  • Beclomethasone
  • Fluticasone
  • Budesonide

Oral:
- Prednisolone

IV:
- Hydrocortisone

32
Q

What are the side effects of corticosteroids?

A

Inhaled = fewer systemic effects than oral

  1. Candidiasis
  2. Hoarseness
  3. Adrenal suppression
  4. Osteoporosis
  5. Growth restriction in children
33
Q

Name 2 combined therapies of corticosteroids with LABA

A
  1. Salmeterol + Fluticasone = Seretide

2. Budesonide + Formoterol = Symbicort

34
Q

How do leukotriene receptor antagonists work? Name an example

A

Leukotrienes are synthesised by a variety of inflammatory cells in the airway (I.e. eosinophils, mast cells, macrophages and basophils)

Leukotriene receptor antagonists block the binding of LTD4 to its receptor on target tissues

Example = Montelukast (singulair)

35
Q

How does sodium cromoglycate work in COPD?

A

Mode of action not completely understood

May inhibit degranulation of mast cells

Less effective than inhaled corticosteroids

36
Q

How is Omalizumab used in COPD?

A

Monoclonal antibody that binds IgE

Add on therapy in severe persistent allergic asthma

Fortnightly SC injections

If no response after 16 weeks, discontinue

37
Q

How are mucolytics used in COPD? Name an example

A

Facilitate expectoration by reducing sputum viscosity

  1. Carbocisteine
    - Anti-inflammatory properties
    - Aids regeneration of damaged mucosal cells
38
Q

Outline the management of chronic asthma

A

Step 1: PRN inhaled B2 agonist

Step 2: Add inhaled steroid (200-800mcg/day)

Step 3: Add LABA, +/- increased steroid dose to 800mcg/day; Consider leukotriene receptor antagonist or SR theophylline

Step 4: Further increase inhaled steroid up to 2000mcg/day; Add 4th drug (leukotriene receptor antaogonist, SR theophylline, or B2 agonist tablets)

Step 5: Daily low dose oral steroid; continue high dose inhaled steroid; refer to specialist

39
Q

How do you assess an acute exacerbation of asthma?

A

Life threatening:

  1. PEF < 33% best or predicted
  2. SpO2 < 92%
  3. PaO2 < 8kPa
  4. Silent chest
  5. Cyanosis
  6. Poor respiratory effort
  7. Arrhythmia
  8. Exhaustion, altered conscious level

Near fatal:
- Raised PaCO2 and/or requiring mechanical ventilation

40
Q

How would you manage a patient with acute exacerbation of asthma?

A

Initial:

  • Sit patient up
  • Give high flow oxygen
  • Nebulised B2 agonists every 15min
  • Nebulised ipratropium (repeat every 4h)
  • Steroids: prednisolone (40mg), hydrocortisone (100mg)

If not responding:

  • Magnesium (1.2-2g IV over 20min)
  • Consider IV aminophylline or B2 agonists
41
Q

What treatments are used for asthma, COPD or both?

A

B2 agonists, Ipratroprium, inhaled corticosteroids and tablet corticosteroids are used for both asthma and COPD. In practice, theophylline is not as commonly used for asthma as it is for COPD, but can be indicated in difficult cases. Magnesium typically is used for treating an acute exacerbation of asthma, and rarely used in an acute exacerbation of COPD.

Leukotriene receptor agonists are only used in asthma, whereas carbocisteine is only used to aid sputum production in COPD, again rarely in Severe Asthma. Sodium cromoglicate is only used for asthma.

42
Q

Can you give some examples of each of the generic names for:

ICS
LABA
LAMA
Combination Inhaler

A

ICS: Clenil, QVAR, pulmicort, Flixotide
LABA: Serevent
LAMA: Spiriva
Combination inhaler: Seretide, Symbicort, Fostair

43
Q

What is the difference between Type 1 and Type 2 respiratory failure?

A

Type I respiratory failure is also known as hypoxaemic failure, and is defined by a PaO2 of less than 8kPa. It indicates a serious underlying pathology with the lungs such as infection, oedema or a shunt.

Type II respiratory failure is also known as ventilatory failure, results when PaCO2 is more than 7. Reduced ventilatory effort can be a result of gas trapping, such as in COPD and severe asthma, due to chest wall deformities, muscle weakness or central causes of respiratory depression.

44
Q

What is the pathological process that leads to Type II respiratory failure in COPD? What physiological compensatory mechanisms occur in the body to reduce the level of acidaemia?

A

In COPD the elastic recoil of the lungs is lost. This causes gas trapping and reduced excretion of carbon dioxide. In the blood, the carbon dioxide combines with water to form carbonic acid. In an acute setting, the increased acid levels in the blood would lower the pH levels and the patient would become unwell very quickly. However when carbon dioxide retention is progressive, as if often the case in chronic COPD, the body can compensate for this by utilising the bicarbonate buffer system of the blood. The kidneys are stimulated to reabsorb more bicarbonate, which acts as a base and neutralises the carbonic acid, thus restoring the pH back to the normal range.

45
Q

What are the clinical features of hypercapnia?

A
  1. Dilated pupils
  2. Bounding pulse
  3. Hand flap
  4. Myoclonus
  5. Confusion
  6. Drowsiness
  7. Coma
46
Q

What are the normal ABG values?

A

PaO2 = 10-13kPa

pH = 7.35-7.45

PaCO2 = 4.5 - 6.0kPa

HCO3- = 22-26kPa

Base excess = -2 to +2

47
Q

What PaO2 value indicates hypoxia?

A

< 8kPa

48
Q

How do you calculate the A-a gradient and what is the normal value?

A

PAO2 (alveolar oxygen) - PaO2 (arterial oxygen) = A-a gradient

Normal A-a gradient = 10
- If > 10 = lung problem (if O2 levels are ≤ 50%)

49
Q

How long does respiratory/metabolic compensation take to occur?

A

Respiratory compensation = quick

Metabolic compensation = days to weeks (if you see this this means the patient has chronic respiratory pathology)

50
Q

What are the main differences between CPAP and NIV (BiPAP)?

A

CPAP:
1. High flow + PEEP

  1. Recruits alveoli
  2. Corrects V/Q mismatch
  3. Used in Type 1 respiratory failure (I.e. pneumonia, sleep apnea, atelectasis, congestive heart failure)

NIV:

  1. Inspiratory push behind each breath + PEEP
  2. Increases tidal volume + decreases CO2
  3. Used in Type 2 respiratory failure (I.e. COPD + asthma exacerbation)
51
Q

Name 5 clinical and pathological features of COPD

A
  1. Breathless on exertion
  2. Hyperinflated chest
  3. Wheeze
  4. Regular sputum production
  5. Smoker/ex-smoker
52
Q

You are undertaking a medication review on one of your patients in a GP surgery. You note that the latest spirometry shows an FEV1 of 59%. The patient is already taking salbutamol prn. What other medications should be considered at this point?

A
  1. Tiotropium inhaler

2. Salmeterol inhaler

53
Q

What clinical features are associated with an exacerbation of COPD?

A
  1. Increased breathlessness
  2. Increased production of sputum
  3. Increased wheeze
54
Q

Name the class of drugs for the following:

  • Salbutamol
  • Theophylline
  • Magnesium
  • Prednisolone
  • Ipratropium
A

Salbutamol = B2 agonist

Theophylline = Phosphodiesterase inhibitor

Magnesium = Ca2+ agonist

Prednisolone = Changes nuclear transcription of cells to reduce inflammation

Ipratropium = anticholinergic antagonist

55
Q

What are the 5 most common infective causes of exacerbations of COPD?

A
  1. Strep. Pneumonia
  2. Viruses
  3. Moraxella catarrhasis
  4. H. influenzae
  5. Pseudomonas aeruginosa
56
Q

When is long term home oxygen therapy (LTOT) indicated in patients with COPD?

A

PaO2 < 7.3kPa on room air

57
Q

Practice prescribing an appropriate ‘handihaler’ for a patient known to use it for treatment of his COPD, selected from the list below. The patient has no known drug allergies.

A

Tiotropium 18mcg handihaler, 1 puff, INH

58
Q

What kind of infection is associated with high neutrophil counts and a very high CRP?

A

Bacterial infection

59
Q

What are 2 side effects of ipratropium?

A
  1. Worsening glaucoma

2. Urinary retention

60
Q

What is the definition of an infective exacerbation of COPD?

A
  1. An increase in volume of sputum

2. An increase in purulence of sputum

61
Q

What are the 3 main causes of a wheeze?

A
  1. COPD
  2. Heart Failure
  3. Pulmonary oedema
62
Q

What occurs to pupil size with CO2 retention?

A

Pupil size increases as CO2 causes vasodilation

63
Q

Name 4 causes of hypercapnic respiratory failure

A
  1. Opioid toxicity
  2. CVA
  3. Post-polio
  4. Scoliosis

Due to alveolar hypoventilation

64
Q

What type of respiratory failure occurs in pneumonia?

A

Most commonly type 1 unless there’s a loss of consciousness then type 2

65
Q

List 8 contraindications for NIV?

A
  1. GCS < 8 (confusion)
  2. pH < 7.25
  3. Somnolence, agitation, lack of co-operation
  4. High risk of gastric aspiration (vomiting)
  5. Facial trauma/deformity
  6. Recurrent gastro-esophageal surgery
  7. Untreated pneumothorax
  8. Pneumonia
66
Q

What are 3 indications for NIV? What is important to remember with NIV?

A
  1. Respiratory acidosis despite controlled oxygen therapy
  2. Moderate to severe breathlessness with accessory muscle use and paradoxical abdominal movement
  3. Respiratory rate > 22

Remember:

  • Need regular ABGs
  • Usually used just for COPD condition not I.e. pneumonia, heart failure
67
Q

Name 2 signs of hypercapnia?

A
  1. Asterixis (flapping tremor)

2. Drowsiness

68
Q

What is the Venturi principle?

A

Bottom of mask draws in a fixed amount of air so you know the proportion of oxygen going into the mask

25, 28, 35, 40, 60% = blue, white, yellow, red, green

year 3 tcds (24 decks)

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